Neural blocking therapy

ABSTRACT

A method and apparatus are disclosed for treating a variety of conditions include treating a disorder associated with neural activity near a region of a brain. In such condition, the method includes placing an electrode to create a field near said region, creating said field with parameters selected to at least partially block neural activity within said field. For treating a tissue sensation, the method includes identifying a target area of tissue to be treated and placing an electrode to create a field near the target area, and creating the field with parameters selected to at least partially block neural activity within the target area. For treating a condition associated with neural activity of a spinal cord, the method includes placing an electrode to create a field near a nerve associated with the spinal cord, and creating the field with parameters selected to at least partially block neural activity within the nerve.

I. BACKGROUND OF THE INVENTION 1. Field of the Invention

This application pertains to method and apparatus for treatingconditions associated with neuronal activity.

2. Description of the Prior Art

a. Neural Stimulation Treatments

The prior art contains numerous examples of treatments involvingstimulation signals to nerves, muscles or organs for treating a widevariety of medical disorders.

U.S. Pat. Nos. 4,702,254 and 5,229,569 (both assigned to Cyberonics,Inc.) describe various central nervous system (CNS) treatments usingelectrical stimulation applied to the vagus nerve. For example, the '254patent describes treatment of epilepsy. The '569 patent describestreatment of neuropsychiatric disorders. U.S. patent application Publ.No. 2003/0144709 (also assigned to Cyberonics, Inc.) describes treatmentof pain through nerve stimulation.

U.S. patent application publication No. 2004/0243205 A1 to Keravel etal. published Dec. 2, 2004 and assigned to Medtronic, Inc., Minneapolis,Minn., USA (incorporated herein by reference) describes a paddle leadwith multiple electrodes. The paddle is placed beneath the skulloverlying a target area of the cerebral cortex. The electrodes recordsomaestheic-evoked potentials. The same electrodes may be used for astimulation therapy.

Nerve stimulation and muscle stimulation have been suggested fortreating gastro-intestinal (GI) disorders. Treatments ofgastrointestinal diseases through nerve stimulation have been suggested.For example, U.S. Pat. No. 6,238,423 to Bardy dated May 29, 2001describes a constipation treatment involving electrical stimulation ofthe muscles or related nerves of the gut. U.S. Pat. No. 6,571,127 toBen-Haim et al. dated May 27, 2003 describes increasing motility byapplying an electrical field to the GI tract. U.S. Pat. No. 5,540,730 toTerry, Jr. et al., dated Jul. 30, 1996 describes a motility treatmentinvolving vagal stimulation to alter GI contractions in response to asense condition indicative of need for treatment. U.S. Pat. No.6,610,713 to Tracey dated Aug. 26, 2003 describes inhibiting release ofa proinflammatory cytokine by treating a cell with a cholinergic agonistby stimulating efferent vagus nerve activity to inhibit the inflammatorycytokine cascade. U.S. Pat. No. 6,622,047 to Barret et al dated Sep. 16,2003 described obesity treatment through vagal stimulation.

b. Neural Blocking

The fore-going treatments are stimulation for treatments. For thoseapplying a signal to a nerve, the signal parameters (pulse width,frequency and amplitude) are selected to initiate neural actionpotentials to be propagated along the nerve to an organ (e.g., brain orstomach).

Not all electrical signals applied to nerves are stimulation signals.Certain parameters can result in a signal that inhibits the nerve orblocks the propagation of action potentials along the nerve.

Many different forms of nerve blocking are known. The present inventionis an improvement upon a neural blocking to avoid antidromic influencesduring stimulation or to otherwise down-regulate nerve activity.Cryogenic nerve blocking of the vagus is described in Dapoigny et al.,“Vagal influence on colonic motor activity in conscious nonhumanprimates”, Am. J. Physiol., 262: G231-G236 (1992). Electrically inducednerve blocking is described in Van Den Honert, et al., “Generation ofUnidirectionally Propagated Action Potentials in a Peripheral Nerve byBrief Stimuli”, Science, Vol. 206, pp. 1311-1312. An electrical nerveblock is described in Solornonow, et al., “Control of Muscle ContractileForce through Indirect High-Frequency Stimulation”, Am. J. of PhysicalMedicine, Vol. 62, No. 2, pp. 71-82 (1983) and Petrofsky, et al.,“Impact of Recruitment Order on Electrode Design for Neural Prostheticsof Skeletal Muscle”, Am. J. of Physical Medicine, Vol. 60, No. 5, pp.243-253 (1981). A neural prosthesis with an electrical nerve block isalso described in U.S. Patent Application Publication No. US2002/0055779 A1 to Andrews published May 9, 2002. A cryogenic vagalblock and resulting effect on gastric emptying are described in PatersonCalif., et al., “Determinants of Occurrence and Volume of TranspyloricFlow During Gastric Emptying of Liquids in Dogs: Importance of VagalInput”, Dig Dis Sci, (2000); 45:1509-1516.

A frequency of the blocking signal is greater than a 200 Hz thresholdand, preferably, greater than 500 Hz. Solomonow, et al. “control ofmuscle contractile force through indirect high-frequency stimulation”,American Journal of Physical Medicine, Volume 62, No. 2, pages 71-82(1983). Higher frequencies of as high as 5,000 Hz result in moreconsistent neural conduction block. Kilgore, et al., “Nerve ConductionBlock Utilizing High-Frequency Alternating Current”, Medical andBiological Engineering and Computing, Vol. 24, pp. 394-406 (2004).

The nerve conduction block is applied with electrical signals selectedto block the entire cross-section of the nerve (for example, bothafferent, efferent, myelinated and non-myelinated fibers) at the site ofapplying the blocking signal (as opposed to selected sub-groups of nervefibers or just afferent and not efferent or vice versa).

c. Use of Neural Blocking in Treatments

U.S. Pat. No. 5,188,104 to Wernicke et. al. Dated Feb. 23, 1993describes sub-selection of fibers in a nerve by selecting a treatmentfrequency by which blocks certain nerve fiber types in the nerve whilestimulating other nerve fiber types. Since certain fibers are stimulatedwhile other fibers are blocked, there is no cross-section inhibition orblocking of the entire nerve and all of its nerve fiber types (forexample, both afferent, efferent, myelinated and non-myelinated fibers).

U.S. Pat. No. 6,684,105 to Cohen et al. dated Jan. 27, 2004 (assigned toBiocontrol Medical Ltd.) teaches collision blocking in which astimulation signal is applied to a nerves and an appropriately timedstimulus is applied to nerve to create neural impulses which collidewith and thereby block propagation of the stimulation signal in a givendirection. No therapy is achieved by the blocking. Such blocking avoidsadverse side effects associated with permitting the stimulation signalpropagating in an undesired direction to an organ not targeted fortherapy.

U.S. patent application Publ. No. 2002/0055779 A1 published May 9, 2002describes applying a high frequency block to a sciatic nerve to blockundesired neural impulses which would otherwise contribute to spasticmovement. With such spasm-inducing signals blocked, a therapy signal isapplied to the muscle to stimulated desired muscle contractions. U.S.patent application Publ. No. 2005/0149148 A1 published Jul. 7, 2005(assigned to Medtronic, Inc.) teaches using a blocking signal to avoidundesired side effect (i.e., pain) otherwise associated with astimulation signal.

The use of a blocking signal as a therapy is described in various patentapplications assigned to EnteroMedics, Inc. These applications pertainto use of a conduction block technology to a nerve for a treatment of avariety of disorders. These applications include the following (allfiled Sep. 29, 2003): U.S. patent application Ser. No. 10/674,330(published Sep. 2, 2004 as Publication No. US 2004/0172086 A1); U.S.patent application Ser. No. 10/675,818 (published Sep. 9, 2004 as USPatent Application Publication No. US 2004/0176812 A1) and U.S. patentapplication Ser. No. 10/674,324 (published Sep. 2, 2004 as US PatentApplication Publication No. 2004/0172085 A1). The same assignee isassigned U.S. patent application Ser. Nos. 10/752,994 and 10/752,940both filed Jan. 6, 2004 with respective publication dates of Aug. 26,2004 and Sep. 2, 2004, Publication Nos. US 2004/0167583 A1 and2004/0172088 A1 .

The foregoing EnteroMedics patent applications describe, in a preferredembodiment, the application of neural conduction block therapy to avagus nerve alone or in combination with a stimulation of the nerve. Theconduction block therapy of the these patent applications includesapplication of an electrical signal with parameters selected todown-regulate vagal activity by creating conditions in which normalnerve propagation potentials are blocked at the application of thesignal on both afferent and efferent nerves fibers of the vagus.Representative treatments described in these applications include thetreatment of obesity, pancreatitis, pain, inflammation, functional GIdisorders, irritable bowel syndrome and ileus.

d. Accommodation

Blockage of a nerve can result in nerve accommodation in which othernerve groups assume, in whole in part, the function of the blockednerve. For example, sub-diaphragm blocking of the vagus nerve may beaccommodated by the enteric nervous system. U.S. patent application Ser.No. 10/881,045 filed Jun. 30, 2004 (published Feb. 17, 2005 asPublication No. US 2005/0038484 A1) (assigned to EnteroMedics, Inc.)notes that a duty cycle of electrical impulses to the nerve to blockneural conduction on the nerve can be adjusted between periods ofblocking and no blocking in order to vary the amount of down regulationof the vagus nerve as well as preventing accommodation by the entericnervous system.

e. Drug Treatments

Many symptoms of Parkinson's disease can be controlled with one of manycurrently available medications. These are divided into several classesof drugs including dopamine agonists, levodopa/decarboxylase inhibitors,anticholinergic agents, MAO-B inhibitors, and COMT(catechol-O-methyltransferase) inhibitors. These medications, whetherused alone or in combination, not only replace the dopamine that hasbeen lost in the brain, but also slow the rate of dopamine loss in thebrain, and/or correct the imbalance between the levels of dopamine andacetylcholine in the brain. While none of these medications are a curefor Parkinson's disease, they can alleviate the symptoms of the diseaseand help its victims manage the disease.

One of the most effective and widely administered medications introducedin the 1970's to relieve symptoms of Parkinson's disease works as adopamine replacement therapy. This drug is known as Sinemet (genericname of levodopa/carbidopa), its active ingredient being L-DOPA(L-3,4-dihydroxyphenylalanine). Levodopa is a generic name given toL-DOPA when it is produced as a drug. Unfortunately, dopamine cannot beadministered directly to patients because it does not cross theblood-brain barrier. Hence, L-DOPA, which is the precursor form ofdopamine, crosses the blood-brain barrier, and can be converted todopamine in the brain, is the molecule of choice. However, due to thepresence of aromatic amino acid decarboxylase (AADS) in the periphery ofthe brain, which will convelt L-DOPA to dopamine before it crosses theblood brain barrier and prevent its passage to the brain, L-DOPA isadministered with carbidopa, an AADS inhibitor. Carbidopa inhibitsperipheral AADS action and thus reduces the amount of levodopa needed.

During the first few months the medication is administered, its benefitsare maximal. However, patients taking Sinemet for a longer period areprone to the “wearing-off” effect, a tendency for the effectiveness ofthe drug to be lost with time. Hence, the dose of Sinemet will oftenhave to be increased with time. Sometimes an “on-off effect,” where thesymptoms become sporadic and unpredictable over a period of time, isalso experienced. Moreover, as the dose of the medication is increased,some patients begin to experience side effects due an increase in braindopamine levels. Some major side effects include anxiety, agitation,dyskinesia, vomiting, low blood pressure, hallucination and nausea(Nadeau 1997). The occurrence of side effects limits the furtherincrease in Sinemet's dosage and at this point, treatment options becomelimited. Fortunately, carbidopa minimizes the incidence of vomiting andnausea. Furthermore, although levodopa/carbidopa treatment decreasesbradykinesia and rigidity, it may not relieve tremor and balance.

Sinemet (unlike most medications that are absorbed into blood throughthe stomach) is absorbed from the small intestine. Anything that delaysthe movement of food from the stomach to the small intestine, such asfoods rich in fat and protein, can reduce the amount of the drugabsorbed. Moreover, levodopa has a very short plasma half-life. Itdisappears from the blood in 60 to 90 minutes. Because it is a type ofamino acid called a large neutral amino acid (LNAA), it attaches itselfduring absorption to carrier molecules in the wall of the intestine andis then carried to the blood. Similarly, once in the blood, carriermolecules carry it across the blood-brain barrier. Amino acids such asisoleucine, leucine, valine, phenylalanine, tryptophan and tyrosinecompete for the carrier with levodopa. Hence, a diet rich in protein canfurther compete with the Sinemet for entry into the brain. Thus, it isimportant to carefully evaluate one's diet when taking Sinemet.

Another medication that can be used alone or in combination with Sinemetis Eldepryl (generic name of selegeline). Selegeline is classified as aMAO-B inhibitor and is often administered in 5 mg capsules to help keepthe Sinemet dose lower over time and therefore extend its administrationperiod. In certain cases, it can delay the need for levodopa therapy byup to a year. By blocking the action of MAO-B, selegeline extends thecapabilities of the dopamine in the synapse, delaying the breakdown ofnaturally occurring dopamine and dopamine administered as L-DOPA.Eldepryl thus slows dopamine loss in the synapse and makes it morelikely that a dopamine will reach its corresponding receptor on thereceiving nerve cell and transmit the correct message down the dopaminecircuit. This is often referred to as dopamine conservation therapy.

During the Fourth International Congress of Movement Disorders held inVienna during the summer of 1996, Eldepryl's benefits when administeredin combination with Sinemet were affirmed. In fact, patients taking thedrug combination were shown to experience motor fluctuations 1.8 yearslater on average than those taking only Sinemet. Another advantage oftaking Eldepryl is that there is no specific dietary restrictionassociated with it if taken at the 5 mg dosage. Selegiline is an easydrug to take and has further been shown to protect thedopamine-producing neurons against the toxicity of MPTP. However,selegiline has its drawbacks. Patients have been known to experienceside effects such as nausea, orthostatic hypotension and insomnia.

Dopamine agonists comprise another general category of drugs. Parlodel(generic name of bromocriptine), Permax (generic name of pergolide) andSymmetrel (generic name of amantadine) are examples. Parlodel and Permaxmimic the action of dopamine by interacting with dopamine receptors in aform of dopamine substitution therapy. These two drugs enter the braindirectly at dopamine receptor sites and prolong the duration ofSinemet's effects. An advantage of this approach is that it is lesslikely to cause dyskinesias (the occurrence of abnormal involuntarymovements that results from the intake of high doses of L-DOPA). This isbecause the actual levels of dopamine do not increase in the brain, asis the case with Sinemet. Rather, a substitute form of dopamine is beingused. However, these two drugs are less effective than L-DOPA indecreasing bradykinesia and rigidity and induce side effects such asparanoia, hallucinations, confusion, nausea and vomiting.

Symmetrel is an anti-viral drug used as a dopamine-releasing therapy incombination with Sinemet. It works by allowing the presynaptic neuron tomore easily release dopamine into the synapse. More recently, it hasbeen suggested that Symmetrel acts by binding to glutamate receptors inthe subthalamic nucleus to help redress the imbalance in basal gangliaactivity due to a deficiency in dopamine in a synergistic manner.Symmetrel is either used alone in the first stages of PD or incombination in the later stages. However, its effectiveness is known towear off in a third to a half of the patients taking it. Furthermore, itinduces side effects such as edema, blurred vision, depression,confusion and mottled skin.

Two new drugs, after having undergone extensive clinical trials, weremade available in 1997. Requip (generic name of ropinirole) and Mirapex(generic name of pramipexole) are dopamine agonists. They are selectivefor the dopamine D3 receptor and are selectively targeted toward thebasal ganglia. Both Requip and Mirapex can be used alone or withlevodopa and both show fewer side effects than other drugs (Lozano etal. 1998).

Artane and Cogentine represent yet another class of drugs. They areclassified as anti-cholinergic agents and are used to restore theimbalance between dopamine and acetylcholine levels in the brain. Theywork to reduce the activity of acetylcholine and hence reduce the tremorand stiffness of muscle that come about as a result of having moreacetylcholine than dopamine in the brain.

Until the introduction of L-DOPA, anti-cholinergic agents were the maintreatments for Parkinson's disease. Now Artane and Cogentine are usuallyadministered in combination with other medications for their therapeuticeffect. While effective, these drugs cart also have side effects such asblurred vision, urinary retention, dry mouth, memory loss, andconstipation. Hence, they are of limited use to the older populationbecause they can cause serious neuropsychiatric side effects.

Tasmar (generic name of tolcapone) is a drug classified as a COMTinhibitor. COMT is a peripheral enzyme that reduces levodopa to a lessactive form. Tasmar, which became available in February 1998, has adifferent action than that of the dopamine agonists, in that when COMTactivity is blocked, dopamine remains in the brain for a longer periodof time. Hence, when administered with levodopa, COMT inhibitors prolongthe duration time of Sinem.

II. SUMMARY OF THE INVENTION

A method and apparatus are disclosed for treating a variety ofconditions. These include treating a disorder associated with neuralactivity near a region of a brain. In such condition, the methodincludes placing an electrode to create a field near said region,creating said field with parameters selected to at least partially blockneural activity within said field. For treating a tissue sensation, themethod includes identifying a target area of tissue to be treated andplacing an electrode to create a field near the target area, andcreating the field with parameters selected to at least partially blockneural activity within the target area. For treating a conditionassociated with neural activity of a spinal cord, the method includesplacing an electrode to create a field near a nerve associated with thespinal cord, and creating the field with parameters selected to at leastpartially block neural activity within the nerve.

III. BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a top plan view of a patient's head and showing an electrodearray according to the present invention in phantom lines positionedbeneath a skull of the patient;

FIG. 2 is a side elevation view of a patient with an electrode patchbeneath the skull of the patient and shown in phantom lines with a leadto a control unit positioned in the patient's neck;

FIG. 3 is a view of a brain of a patient shown in lateral cross-sectionand with a patch according to the present invention residing between theskull and the surface of the patient's brain over a cortex of thepatient's brain;

FIG. 4 is a plan view of an electrode patch according to the presentinvention;

FIG. 5 is an anterior-posterior, cross-sectional view of a patient'sbrain showing an alternative embodiment of electrodes placed on acatheter advanced through the ventricle of the brain;

FIG. 6 is a plan view of inside surfaces of an upper arm and forearm andhand of a patient with an alternative embodiment of the presentinvention positioned surrounding a target area for needle insertion;

FIG. 7 is a side elevation view of a section of the electrode patch ofFIG. 6;

FIG. 8 is a graphical presentation of representative waveforms accordingto the present invention for energizing the electrodes of FIG. 6;

FIG. 9 is an illustration of a patient's finger showing electrodes onthe opposite side of a target area at the fingertip of the patient;

FIG. 10 illustrates electrodes on mucosal tissue on opposite sides of atooth to apply a blocking signal;

FIG. 11 is a cross-section view of a vertebral body and showinganatomical components and a blocking signal electrode on a dorsal root;

FIG. 12 is a schematic longitudinal, side-sectional showing of a segmentof a spine with a catheter placement of an electrode on a dorsal root;and

FIG. 13 is an anterior-posterior schematic representation of a segmentof a spine with blocking signal electrodes shown in two positions.

IV. DESCRIPTION OF A PREFERRED EMBODIMENT

With reference now to the various drawing figures in which identicalelements are identically numbered, preferred embodiments of the presentinvention will now be described.

A. Central Nervous System (CNS) Treatment

Certain disorders (e.g., epilepsy and Parkinson's disease and othermotor disorders of CNS origin) are believed to be associated withhormonal imbalance.

Movement disorders associated with cerebral activity are not fullyunderstood. However, certain disorders such as epilepsy and Parkinson'sdisease are believed to be associated with an imbalance of hormonalproduction deep within the brain.

For example, certain regions deep within the brain produce the hormonesglutamate and dopamine. Glutamate enhances conductivity of the nervecells of the brain while dopamine reduces or inhibits such conductivity.

With reference to FIG. 3, dopamine is produced within a region of thebrain known as the substantia nigra SN. Glutamate is produced in thethalamus region of the brain, which includes the ventral anteriornucleus VAN, the ventral lateral nucleus VLN and the centromediannucleus CN. The produced hormones are projected throughout the brainincluding to the cortex which is the outer region of the brain near theback of the head and illustrated generally by C in FIG. 3.

The projection to the cortex C of the glutamate is believed to flow fromproduction of glutamate in the ventral anterior nucleus VAN. Suchprojection is illustrated by the arrow A_(G) in FIG. 3. The projectionof dopamine to the cortex is believed to flow from the substantia nigraSN with such projection illustrated in FIG. 3 by the arrow A_(D).

The presence of dopamine and glutamate in the cortex C alter theconductivity of the nerve cells in the cortex C. Certain motor disorderssuch as epilepsy and Parkinson's disease, are believed to be associatedwith a deficiency of dopamine production which results in excessivelyenhanced conductivity in the cortex since the enhancing hormone,glutamate, is disproportionately high relative to the inhibitingconductivity hormone, dopamine.

The present invention compensates for hormonal imbalance resulting inexcessive conductivity by altering the conductivity at the cortex. Theconductivity of the cortex and electrical activity of the cortexcontrols motor functions of the patient.

The present invention is a patch electrode 10, which is placed beneaththe skull of the patient between the skull S and the cortex C (FIG. 3).The patch electrode 10 includes a flexible flat substrate 12 ofelectrically insulating material such as silicone or the like. Exposedon one surface of the substrate 12 are a plurality of electricallyconductive electrodes, which, in a preferred embodiment, are arranged inan array of rows and columns.

In the specific examples shown in FIGS. 3 and 4, there is a first rowcontaining electrodes E_(1,1) through E_(1,5). The second row containsfive electrodes E_(2,1) through E_(2,5). The third row containselectrodes E_(3,1) through E_(3,5). The fourth row contains electrodesE_(4,1) through E_(4,5). The fifth row contains electrodes E_(5,1)through E_(5,5). The patch 10 is dimensioned for the array of electrodesto cover at least a portion of the cortex C of the brain and with theelectrodes of the array in electrically conductive contact with thecortex C.

As illustrated in FIGS. 1 and 2, the patch electrode 10 is placed overthe cortex beneath the skull on either the left (FIG. 1) or right (FIG.2) of the brain. In FIG. 1, the top of a patient's head H is shown withan anterior-posterior axis A-P separating the patients' left L and rightR sides.

As shown in FIG. 2, a lead 16 from the patch electrode 10 may betunneled between the skull S and the brain B through the base of theskull and terminated at a control unit 20 which may be positioned withinthe neck or implanted lower in the patient such in the shoulder orclavicle area or the like. The lead 16 is a highly flexible conductorcontaining individual conductors for each of the electrodes of the arrayof the patch 10 and encased within a highly flexible insulative materialsuch as silicone or the like.

The controller 20 may be an implantable pulse generator (with separatepower source such as either rechargeable batteries or replaceablebatteries) or may be a control unit, which receives power and pacingsignals from an external control unit, which transmits via radiofrequency transmission to the controller 20. For the purpose of thisdescription, the controller 20 will be treated as a completely containedcontroller having both logic circuits and power source. It will beappreciated that such controllers may be also programmable from externalprogrammable sources as is known in the art for controlling implantablepulse generators for cardiac pacing.

The circuitry of the controller 20 permits energizing selective ones ofthe electrodes of the array in bipolar electrode pairs. For example,electrodes E_(5,1) and E_(4,2) may be energized with oppositelypolarized waveforms to create an electrical field F₁ between theelectrodes E_(5,1) and E_(4,2). By oppositely charged waveforms it willbe appreciated that electrode E_(5,1) is positively charged whileE_(4,2) is negatively charged and E_(5,1) is negatively charged whileE_(4,2) is positively charged. When the electrode pair E_(5,1) andE_(4,2) is charged to create the field F₁, all remaining electrodes maybe inactive or otherwise charged to create more complex electricalfields.

FIG. 4 illustrates a field F₂ created between electrode pairs E_(2,2)and E_(2,4) and a field F₃ between electrode pairs E_(1,1) and E_(5,5).While multiple electrode pairs may be simultaneously charged, thecontroller 20 may also control the electrodes so that the waveformapplied to the electrodes has a built-in delay period such that aparticular electrode pair is not charged and in its delay period, whileother electrode pairs are being charged. Accordingly, multiple pairs ofelectrodes may be charged with the waveforms of the electrode pairsbeing nested so that only one electrode pair is charged at any one unitof time. An example of a nested set of waveforms will be laterdescribed.

Preferably, the waveform selected is a blocking waveform to blockneuronal activity. For example, the frequency of the field will have apulse width selected for the generated field to have a frequency inexcess of a 200 Hz threshold as described by Solomonow (articlepreviously described) and, more preferably, 5,000 Hz or higher asdescribed in Kilgore (article previously described). A 5,000 Hz signalwill have a pulse width of about 100 microseconds. A representativeamplitude for such signals would be 0.2 to 8 mA.

The effect of applying a blocking signal to the cortex reduces theexcessive electrical activity otherwise associated with a dopaminedeficiency. Further, the therapy of the present invention is localizedto the area of interest, namely, the cortex region of the brain, whichcontributes to the symptoms of motor disorders. Other regions of thebrain are not affected and no systemic drug is given to the patient.

The programming of the controller 20 may permit altering the selectedindividual electrodes, which form an electrode pair. Any two electrodeson the patch 10 may be formed to a pair to create a field between thepair. As a result, at time of placement of the patch 10, the patch neednot be precisely placed to achieve an interruption or inhibition ofelectrical activity in the cortex. Instead, different permutations ofcoupled electrode pairs may be tested to observe patient responsepost-surgery.

The forgoing has illustrated use of the blocking signals to compensateand down regulate cortex electrical conductivity in response to dopaminedeficiency. FIG. 5 illustrates use of stimulation signals to result inlocalized production of dopamine. In FIG. 5, a catheter 30 is advancedinto the ventricles of the brain with a distal tip 32 positioned in theregion of the hypothalamus of the brain. The tip 32 includes anelectrode pair E_(A) and E_(B), which form a bipolar electrode pair. Theelectrodes are individually electrically connected to a controller (notshown but such as controller 20 previously described) for creating adesired waveform (as will be described). The controller provides theelectrodes with either a stimulation signal (for example 20 Hz or anyother signal less than 200 Hz) or a blocking signal as previouslydescribed. Energizing the electrodes with a stimulation signal can betested on a particular patient to note any increase in dopamineproduction and result in cortex activity. Similarly, a blocking signalcan be applied to note any reduction in glutamate production.

B. Peripheral Nervous System Treatment

The use of blocking signals as described may be used to alleviate painon the surface of the skin for a wide variety of applications. Forexample, FIGS. 6 and 7 illustrate a patch 110 which may be placed on theskin surrounding a target area T associated with pain.

In the particular illustration of FIG. 6, a patient's required to giveblood samples frequently require a needle injection into the interiorsurface of the arm to insert a needle into a vein between the upper armUA and the forearm FA. The health care technician's identification ofthe particular vein for puncture is identified and circled by a targetarea T in phantom lines in FIG. 6.

A patch 110 is a ring-shaped substrate 112 sized to surround the targetarea T but otherwise permits access to the target area T by a needle(not shown) for drawing blood or the like. An undersurface of thesubstrate 112 contains diametrically opposite electrode pairs E_(1,A),E_(1,B) and E_(2,A), E_(2,B) and E_(3,A), E_(3,B). The electrodes areindividually electrically connected to a controller (not shown but suchas controller 20 previously described) for creating a desired waveform(as will be described). Between the electrodes adhesive layers 114 areprovided to secure the patch 110 in place on the patient's skinsurrounding the target area T.

The individual electrode pairs are bipolar electrode pairs, which may beprovided with a blocking signal as previously described. For example,the electrode pair E_(1,A), E_(1,B) may be provided with a firstwaveform W₁ illustrated in FIG. 8. The electrode pair E_(2,A), E_(2,B)may be provided with a second waveform W₂ and electrode pairs E_(3,A),E_(3,B) may be provided with a third waveform W₃ in FIG. 8.

Each of the waveforms W₁, W₂ and W₃ are identical differing only intheir timing. The waveforms are preferably blocking waveforms having afrequency in excess of a few hundred Hz threshold and more preferablyhaving a frequency of about 5,000 Hz. With such a frequency, thewaveforms have a pulse duration D of 100 microseconds. Preferably, eachcycle of the waveform has a delayed period DP between the pulses withthe duration of the delay period DP equal to two complete cycles (i.e.,four pulse durations D or 400 microseconds). The amplitude of the pulseA may be any suitable amplitude to encourage current flow between theelectrode pairs. To drive current across the skin, higher energy levelsare anticipated (e.g., voltages up to about 35 volts and currents up to25 mA.

The waveforms are offset relative to one another so that when any oneelectrode pair is receiving a pulse, the other electrode pairs areinactive resulting in three nested waveforms as illustrated in FIG. 8.Such waveforms create an electrical field between the diametricallyopposed electrodes of a particular pair with the field passing throughthe target area T to block neuronal activity within the target area.Accordingly, when the electrodes are energized with the blocking signalsas described, pain is not sensed during needle insertion into the targetarea T.

It will be appreciated in FIG. 6 the apparatus 110 will further includeelectrical leads to a control unit both of which are not shown for easeof illustration.

FIG. 9 illustrates an alternative application where two electrodes E₁ E₂are placed on opposite sides of a target area T near the fingertip of apatient's finger F. For ease of illustration, a substrate for theelectrodes is not shown. The electrodes are individually electricallyconnected to a controller (not shown but such as controller 20previously described) for creating a desired waveform. The applicationof FIG. 9 is particularly useful for numbing a fingertip prior tolancing the fingertip for a blood sample for periodic blood sugar testsby diabetic patients.

FIG. 10 illustrates a still further embodiment where electrodes E₁ andE₂ are placed on opposite sides of the gum of the patient overlyingmucosal tissue MT on opposite sides of a tooth T. Application of ablocking signal as previously described to the electrodes creates ablocking field to block nerves within the mucosal tissue for treatmentof pain associated with gums or teeth or to precondition the tissueprior to injection of local anesthetics such as Novocain or Lydacain orother procedure occurring at the tissue.

C. Spinal Cord Treatment

FIGS. 11-13 illustrate application of the present invention to thespinal cord. By way of anatomical background, FIG. 11 shows, in crosssection, a spinal cord SC position between an anterior vertebral bodyAVB and a posterior vertebral body PVB. The patient's anterior-posterioraxis A-P is shown separating the patient's right R and left L sides.

The spinal cord SC is shown enclosed within a dural layer D withopposing surfaces of the spinal cord SC and the dural D defining asubanachroid space SAS. Extending laterally away from the spinal cordare left and right ventral roots LVR, RVR and right and left dorsalroots RDR, LDR. Also illustrated is a ganglion G. The spinal cord SC isillustrated as having identifiable areas of afferent and efferent fibersincluding ascending pathways AP areas and descending pathways DP areas.

According to the present invention, an electrode E is advanced eitherthrough open surgical or minimally invasive techniques into thesubanachroid space SAS and positioned on a root such as the right dorsalroot RDR. Application of a blocking signal to the electrode E blockssignals such as pain signals from the dorsal root the spinal cord SC.While a single monopolar electrode E is shown in FIG. 11, it will beappreciated that multiple electrodes including bipolar electrodes may beplaced on the roots. For spinal treatments, such blocking signal may beas previously described and, preferably, has a frequency in excess of3,000 Hz and more preferably about 5,000 Hz or more.

FIG. 12 is shown in vertical cross section with multiple vertebralbodies and with a spinal cord extending between the vertebral bodies.For ease of schematic illustration, the dorsal roots are shown extendingbetween the anterior bodies. It will be appreciated that such rootsextend laterally from the spinal cord.

A catheter C is shown in phantom lines for advancing an electrode to adorsal root for placing the electrode on the dorsal root. The electrodelead extends from the electrode through implantable or external pulsegenerator as previously described.

FIG. 13 illustrates an electrode E (the upper electrode E in the view ofFIG. 13) placed on a dorsal root either surgically or through catheterdelivery as previously described. Further, FIG. 13 shows an electrode E(the lower electrode E in the view of FIG. 13) placed overlying thespinal cord over a target area AP, In the example of FIG. 13, the targetarea AP is an identified area of ascending pathways for application of ablocking signal to the ascending pathways for blocking transmission ofneural signals to the brain. The electrode is supported on a sling Swhich is mounted on the left and right dorsal roots. It will beappreciated that the electrode so supported can be positioned over anyarea of the spinal cord to affect any desired area of ascending pathwaysor descending pathways. The electrodes are individually electricallyconnected to a controller (not shown but such as controller 20previously described) for creating a desired waveform.

With the foregoing detailed description of the present invention, it hasbeen shown how the objects of the invention have been attained in apreferred manner. Modifications and equivalents of disclosed conceptssuch as those which might readily occur to one skilled in the art, areintended to be included in the scope of the claims which are appendedhereto.

1-10. (canceled)
 11. An apparatus for treating pain comprising: a) atleast two bipolar electrodes and adapted to overlie a dorsal region ofthe spinal cord; and b) an implantable rechargeable controller that iselectrically connected to the at least two bipolar electrodes andprovides electrical signals having a frequency of at least 3,000 Hz toeach of the two electrodes to form an electric field between the atleast two bipolar electrodes that at least partially blocks transmissionof pain signals along ascending pathways in the spinal cord.
 12. Theapparatus of claim 11, wherein the implantable rechargeable controllerprovides bipolar charge balanced electrical signals.
 13. The apparatusof claim 11, wherein the frequency is at least 5000 Hz.
 14. A method oftreating pain in the spinal cord comprising: a) placing at least twobipolar electrodes over a dorsal region of the spinal cord; and b)applying electrical signals having a frequency of at least 3,000 Hz toeach of the two bipolar electrodes via an implantable rechargeablecontroller to form an electrical field between the at least two bipolarelectrodes that at least partially blocks transmission of pain signalsalong ascending pathways of the spinal cord.
 15. The method of claim 14,wherein the implantable rechargeable controller provides bipolar chargebalanced electrical signals.
 16. The method of claim 14, wherein thefrequency is at least 5000 Hz.